Rheumatology and Immunology — MCQs
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Which of the following is an ANCA negative vasculitis?
A 40-year-old male complains of exquisite pain and tenderness over the left ankle. There is no history of trauma. The patient is taking a mild diuretic for hypertension. On examination, the ankle is very swollen and tender. There are no other physical examination abnormalities. What is the next step in management?
Which of the following is NOT an indication for intravenous immunoglobulin (IVIg)?
A 65-year-old man develops the onset of severe right knee pain over 24 hours. The knee is red, swollen, and tender. The patient does not have fever or systemic symptoms; he has never had severe joint pain before. Plain film of the knee shows linear calcification of the articular cartilage without destructive change. Definitive diagnosis is best made by which of the following?
What proportion of patients with Wegener's granulomatosis will have antibodies to Proteinase-3?
Which of the following statements is false regarding Familial Mediterranean fever?
All of the following are true in respect of angioneurotic edema EXCEPT?
What is the causative agent for rheumatoid arthritis?
Urethritis is seen in which of the following conditions?
What is the most common presentation of Wegener's granulomatosis?
Rheumatology and Immunology Indian Medical PG Practice Questions and MCQs
Question 71: Which of the following is an ANCA negative vasculitis?
- A. Wegener granulomatosis
- B. Churg-Strauss syndrome
- C. Polyarteritis nodosa (Correct Answer)
- D. Microscopic polyangiitis
Explanation: The classification of systemic vasculitis is primarily based on the size of the vessels involved and the presence of specific biomarkers like **Anti-Neutrophil Cytoplasmic Antibodies (ANCA)** [2]. **1. Why Polyarteritis Nodosa (PAN) is the correct answer:** Polyarteritis nodosa is a **medium-vessel vasculitis**. By definition, it is **ANCA-negative**. It is characterized by necrotizing inflammation of medium-sized or small arteries without glomerulonephritis or vasculitis in arterioles, capillaries, or venules. A key diagnostic feature is its association with **Hepatitis B virus (HBV)** infection and the presence of "rosary sign" (microaneurysms) on angiography. **2. Why the other options are incorrect:** Options A, B, and D belong to the category of **ANCA-Associated Vasculitides (AAV)**, which primarily affect small vessels: * **Wegener Granulomatosis (Granulomatosis with Polyangiitis - GPA):** Strongly associated with **c-ANCA** (anti-PR3). It typically involves the triad of upper respiratory tract, lungs, and kidneys. * **Churg-Strauss Syndrome (Eosinophilic Granulomatosis with Polyangiitis - EGPA):** Associated with **p-ANCA** (anti-MPO) [1]. It is characterized by asthma, peripheral eosinophilia, and granulomatous inflammation [1]. * **Microscopic Polyangiitis (MPA):** Strongly associated with **p-ANCA** (anti-MPO). Unlike PAN, it involves small vessels (capillaries) and frequently causes pauci-immune necrotizing glomerulonephritis. **High-Yield Clinical Pearls for NEET-PG:** * **PAN Rule of Thumb:** "PAN is ANCA-negative and spares the lungs." * **c-ANCA (Cytoplasmic):** Targets Proteinase-3 (PR3); specific for GPA. * **p-ANCA (Perinuclear):** Targets Myeloperoxidase (MPO); seen in MPA, EGPA, and Primary Sclerosing Cholangitis [1]. * **Microaneurysms:** In PAN, these are commonly found in renal, mesenteric, or hepatic arteries.
Question 72: A 40-year-old male complains of exquisite pain and tenderness over the left ankle. There is no history of trauma. The patient is taking a mild diuretic for hypertension. On examination, the ankle is very swollen and tender. There are no other physical examination abnormalities. What is the next step in management?
- A. Begin colchicine and broad-spectrum antibiotics
- B. Obtain uric acid level and perform arthrocentesis (Correct Answer)
- C. Begin allopurinol if uric acid level is elevated
- D. Obtain ankle x-ray to rule out fracture
Explanation: ### **Explanation** **1. Why Option B is Correct:** The clinical presentation of acute, exquisite pain, swelling, and tenderness in a single joint (monoarthritis) in a middle-aged male is highly suggestive of **Gouty Arthritis**. The use of **diuretics** (like Thiazides) is a classic trigger for gout as they decrease renal urate excretion [1]. The **gold standard** for diagnosing any acute monoarthritis is **Arthrocentesis (Joint Fluid Analysis)**. This is crucial to: * Confirm gout by identifying **monosodium urate crystals** (needle-shaped, negatively birefringent). * Rule out **Septic Arthritis**, which is a surgical emergency and can mimic gout perfectly [2]. While serum uric acid levels are often checked, they can be normal during an acute attack; however, they serve as a baseline for long-term management. **2. Why Other Options are Incorrect:** * **Option A:** Antibiotics should not be started empirically without synovial fluid analysis confirming infection. Colchicine is used for treatment, but diagnosis must come first. * **Option C:** **Allopurinol** (a xanthine oxidase inhibitor) should **never** be started during an acute attack [1]. Sudden changes in urate levels can worsen or prolong the inflammation. It is used for long-term prophylaxis only after the acute episode resolves. * **Option D:** In the absence of trauma, a fracture is highly unlikely. X-rays in early gout usually show only soft tissue swelling and are not diagnostic. **3. NEET-PG High-Yield Pearls:** * **Most common joint involved:** 1st Metatarsophalangeal joint (Podagra) [1]. * **Radiology:** "Punched-out" erosions with overhanging edges (Martel’s sign) are seen in chronic tophaceous gout. * **Drug of Choice (Acute):** NSAIDs (e.g., Indomethacin) or Colchicine. * **Drug of Choice (Chronic):** Allopurinol (Febuxostat if renal impairment is present) [1]. * **Polarizing Microscopy:** Gout = Yellow when parallel to the axis (Negative birefringence); Pseudogout = Blue when parallel (Positive birefringence).
Question 73: Which of the following is NOT an indication for intravenous immunoglobulin (IVIg)?
- A. Idiopathic thrombocytopenic purpura (ITP)
- B. Kawasaki disease
- C. Acute infective polyneuritis
- D. Systemic lupus erythematosus (SLE) (Correct Answer)
Explanation: **Explanation:** The correct answer is **Systemic lupus erythematosus (SLE)**. While IVIg is used in various autoimmune and inflammatory conditions, it is **not** considered a standard or first-line indication for SLE [1]. SLE is primarily managed with corticosteroids, hydroxychloroquine, and immunosuppressants (like mycophenolate mofetil or cyclophosphamide) or biologics (like Belimumab). **Why the other options are incorrect (Indications for IVIg):** * **Idiopathic Thrombocytopenic Purpura (ITP):** IVIg is a first-line treatment, especially when a rapid increase in platelet count is required (e.g., pre-surgery or life-threatening bleed). It works by blocking Fc receptors on splenic macrophages, preventing platelet destruction. * **Kawasaki Disease:** High-dose IVIg administered within the first 10 days of fever onset is the gold standard treatment. It significantly reduces the risk of developing **coronary artery aneurysms**. * **Acute Infective Polyneuritis (Guillain-Barré Syndrome):** IVIg is a mainstay of treatment, equivalent in efficacy to plasmapheresis. It helps neutralize pathogenic autoantibodies and modulate complement activation. **NEET-PG High-Yield Pearls:** 1. **Mechanism of Action:** IVIg provides passive immunity, neutralizes circulating autoantibodies, and inhibits complement-mediated damage. 2. **Other Key Indications:** Dermatomyositis (refractory), Myasthenia Gravis (crisis), Chronic Inflammatory Demyelinating Polyneuritis (CIDP), and Common Variable Immunodeficiency (CVID). 3. **Side Effect:** A classic board-favorite side effect of IVIg is **Aseptic Meningitis**. 4. **Contraindication:** Patients with **IgA deficiency** are at risk of anaphylaxis when given IVIg due to the presence of anti-IgA antibodies.
Question 74: A 65-year-old man develops the onset of severe right knee pain over 24 hours. The knee is red, swollen, and tender. The patient does not have fever or systemic symptoms; he has never had severe joint pain before. Plain film of the knee shows linear calcification of the articular cartilage without destructive change. Definitive diagnosis is best made by which of the following?
- A. Serum uric acid
- B. Serum calcium
- C. Arthrocentesis and identification of positively birefringent rhomboid crystals (Correct Answer)
- D. Rheumatoid factor
Explanation: This clinical scenario describes a classic presentation of **Pseudogout** (Calcium Pyrophosphate Deposition Disease or CPPD) [1]. ### **Why Option C is Correct** The definitive diagnosis of any crystal-induced arthropathy requires **arthrocentesis** (joint fluid aspiration) and polarized light microscopy. In CPPD, the synovial fluid reveals **rhomboid-shaped crystals** [3] that exhibit **weak positive birefringence** (they appear blue when parallel to the compensator axis). The radiographic finding of "linear calcification of articular cartilage" is known as **chondrocalcinosis**, a hallmark of CPPD [1], [3]. ### **Why Other Options are Incorrect** * **A. Serum uric acid:** This is used to screen for Gout (monosodium urate crystals) [3]. However, the crystals in Gout are needle-shaped and negatively birefringent. Furthermore, serum uric acid levels can be normal during an acute attack. * **B. Serum calcium:** While CPPD can be associated with metabolic conditions like hyperparathyroidism, serum calcium levels do not diagnose the acute joint pathology. * **D. Rheumatoid factor:** RF is a screening tool for Rheumatoid Arthritis, which typically presents as a chronic, symmetric, polyarticular small-joint involvement, rather than an acute monoarthritis [2] with chondrocalcinosis. ### **NEET-PG High-Yield Pearls** * **The "3 Hs" of CPPD associations:** **H**yperparathyroidism, **H**emochromatosis, and **H**ypomagnesemia (also Hypothyroidism). * **Radiology:** Chondrocalcinosis is most commonly seen in the **knee** (meniscus), **wrist** (triangular fibrocartilage), and **symphysis pubis** [3]. * **Crystal Comparison:** * **Gout:** Needle-shaped, **N**egatively birefringent (**Y**ellow when parallel—mnemonic: **NY**) [3]. * **Pseudogout:** Rhomboid-shaped, **P**ositively birefringent (**B**lue when parallel—mnemonic: **PB**) [3]. * **Treatment:** Acute management involves NSAIDs, colchicine, or intra-articular steroids.
Question 75: What proportion of patients with Wegener's granulomatosis will have antibodies to Proteinase-3?
- A. 10%
- B. 50%
- C. 90% (Correct Answer)
- D. 100%
Explanation: **Explanation:** **Wegener's Granulomatosis** (now officially known as **Granulomatosis with Polyangiitis - GPA**) is a small-vessel vasculitis characterized by the triad of upper respiratory tract involvement, lower respiratory tract involvement, and glomerulonephritis. **1. Why 90% is correct:** The hallmark serological marker for GPA is the **Antineutrophil Cytoplasmic Antibody (ANCA)**. Specifically, GPA is associated with **c-ANCA** (cytoplasmic pattern), where the primary target antigen is **Proteinase-3 (PR3)**. In patients with active, generalized (systemic) disease, the sensitivity of c-ANCA/anti-PR3 is approximately **90%**. This makes it a highly specific and sensitive diagnostic tool for the condition. **2. Why other options are incorrect:** * **10%:** This is far too low. While ANCA may be negative in very early or localized disease (limited to the upper respiratory tract), it is positive in the vast majority of systemic cases. * **50%:** This represents the sensitivity of ANCA in patients with "limited" GPA (disease confined to the respiratory tract without renal involvement), but for the classic presentation of the disease, the percentage is much higher. * **100%:** In medicine, few tests are 100% sensitive. A small subset of patients (approx. 10%) remains "ANCA-negative" despite biopsy-proven GPA. **High-Yield Clinical Pearls for NEET-PG:** * **c-ANCA = Anti-PR3:** Associated with GPA (Wegener's). * **p-ANCA = Anti-MPO (Myeloperoxidase):** Associated with Microscopic Polyangiitis (MPA) and Churg-Strauss Syndrome (EGPA). * **Biopsy Gold Standard:** While ANCA is a great screening tool, the definitive diagnosis requires a biopsy showing **necrotizing granulomatous inflammation**. * **Treatment:** Induction is typically with Corticosteroids + Cyclophosphamide (or Rituximab).
Question 76: Which of the following statements is false regarding Familial Mediterranean fever?
- A. Form of hereditary amyloidosis
- B. Excessive production of TNF-alpha (Correct Answer)
- C. Autosomal recessive inheritance
- D. Mutation affecting pyrin protein
Explanation: Explanation: Familial Mediterranean Fever (FMF) is the most common hereditary autoinflammatory syndrome. The correct answer is B because the primary cytokine involved in FMF is Interleukin-1 beta (IL-1β), not TNF-alpha. 1. Why Option B is False: FMF is caused by mutations in the MEFV gene, which encodes the protein pyrin. Pyrin normally regulates the inflammasome complex. Mutated pyrin leads to the uncontrolled activation of the NLRP3 inflammasome, resulting in the excessive production and release of IL-1β. This triggers the characteristic recurrent episodes of fever and serositis (peritonitis, pleuritis, or synovitis). 2. Why Option A is True: FMF is a major cause of AA amyloidosis (secondary amyloidosis) [1]. Chronic, uncontrolled inflammation leads to high levels of Serum Amyloid A (SAA), which deposits in organs, most notably the kidneys, leading to nephrotic syndrome and renal failure [2]. 3. Why Option C is True: FMF follows an autosomal recessive pattern of inheritance, typically seen in populations of Mediterranean descent (Sephardic Jews, Turks, Armenians, and Arabs). 4. Why Option D is True: As mentioned, the MEFV gene mutation directly affects the pyrin protein, impairing its ability to inhibit the inflammatory response. High-Yield Clinical Pearls for NEET-PG: * Drug of Choice: Colchicine is the mainstay of treatment; it prevents acute attacks and, more importantly, prevents the development of AA amyloidosis [1]. * Clinical Presentation: Recurrent, self-limiting episodes of fever (lasting 1–3 days) accompanied by sterile peritonitis (mimicking acute abdomen) or pleuritis. * Erysipeloid Erythema: A pathognomonic skin rash (red, swollen area typically on the lower legs or dorsum of the foot) seen in FMF.
Question 77: All of the following are true in respect of angioneurotic edema EXCEPT?
- A. It is caused by deficiency of complement proteins
- B. It manifests as pitting edema (Correct Answer)
- C. It is more common in females
- D. It is an autosomal dominant disorder
Explanation: Angioneurotic edema (Hereditary Angioedema - HAE) is characterized by episodic, localized swelling of the deep dermis, subcutaneous tissues, or submucosa. **Why Option B is the Correct Answer (The "Except"):** Angioedema manifests as **non-pitting edema**. Unlike systemic conditions (like heart failure or renal failure) where fluid accumulates in the interstitial space due to hydrostatic or oncotic pressure changes [2], angioedema is caused by increased vascular permeability (mediated by bradykinin or histamine). This leads to rapid, deep tissue swelling that is firm and does not leave an indentation upon pressure. **Analysis of Other Options:** * **Option A (Deficiency of complement proteins):** HAE is caused by a deficiency or dysfunction of **C1 esterase inhibitor (C1-INH)**. This leads to the consumption of C4 and C2; thus, low C4 levels are a classic screening marker. * **Option C (More common in females):** While the genetic inheritance is equal, clinical attacks are often more frequent and severe in females, frequently triggered by exogenous estrogens (OCPs) or endogenous hormonal shifts (puberty, menstruation). * **Option D (Autosomal dominant):** HAE (Types I and II) is inherited in an **autosomal dominant** pattern, though roughly 25% of cases arise from de novo mutations. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mediator:** The primary mediator in HAE is **Bradykinin**, not histamine [1]. Therefore, it does **not** respond to antihistamines or steroids. 2. **Classic Presentation:** Recurrent episodes of non-pitting edema, colicky abdominal pain (bowel wall edema), and potentially fatal laryngeal edema. 3. **Diagnosis:** Low **C4 levels** (best initial screening). C1-INH levels/function are then measured for confirmation. 4. **Treatment:** Acute attacks are treated with **C1-INH concentrate**, **Ecallantide** (kallikrein inhibitor), or **Icatibant** (bradykinin B2 receptor antagonist) [1]. Fresh Frozen Plasma (FFP) is used if specific concentrates are unavailable.
Question 78: What is the causative agent for rheumatoid arthritis?
- A. Mycoplasma (Correct Answer)
- B. Mycobacterium avium
- C. Yersinia
- D. Herpes virus
Explanation: **Explanation:** The exact etiology of Rheumatoid Arthritis (RA) remains multifactorial, involving a complex interplay between genetic predisposition (HLA-DR4) and environmental triggers. Among infectious agents, **Mycoplasma** species (particularly *Mycoplasma fermentans*) have been frequently implicated in the pathogenesis. The underlying medical concept is that Mycoplasma can act as a "superantigen" or trigger chronic inflammation through molecular mimicry, leading to the production of autoantibodies in genetically susceptible individuals. **Analysis of Options:** * **Mycoplasma (Correct):** Studies have isolated Mycoplasma DNA from the synovial fluid of RA patients. Its ability to persist intracellularly and modulate the host immune response makes it a primary suspect in triggering the chronic synovitis characteristic of RA. * **Mycobacterium avium:** While certain Mycobacteria are linked to autoimmune phenomena, *M. avium* is primarily associated with opportunistic infections in immunocompromised patients (e.g., HIV) rather than RA. * **Yersinia:** *Yersinia enterocolitica* is a classic trigger for **Reactive Arthritis**, not Rheumatoid Arthritis. It typically follows a gastrointestinal infection. * **Herpes virus:** While EBV (a herpes virus) is studied for its role in RA due to its effect on B-cells, Mycoplasma is the more traditionally cited "causative agent" in the context of this specific question's classic medical curriculum. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Association:** Strongly linked to **HLA-DR4** (specifically the "shared epitope"). * **Environmental Trigger:** **Smoking** is the most significant environmental risk factor and is linked to the citrullination of proteins. * **Other Pathogens:** *Porphyromonas gingivalis* (periodontal disease) and *Proteus mirabilis* are also high-yield organisms associated with RA pathogenesis. * **Antibody Specificity:** While Rheumatoid Factor (RF) is sensitive, **Anti-CCP** (Anti-cyclic citrullinated peptide) is the most specific marker for RA.
Question 79: Urethritis is seen in which of the following conditions?
- A. Reiter's syndrome (Correct Answer)
- B. Gout
- C. Rheumatoid arthritis
- D. Polyarteritis nodosa (PAN)
Explanation: The correct answer is **Reiter's syndrome** (now more commonly referred to as **Reactive Arthritis**). **1. Why Reiter’s Syndrome is Correct:** Reiter’s syndrome is a classic form of seronegative spondyloarthropathy that typically develops following a gastrointestinal (e.g., *Salmonella, Shigella*) or urogenital (e.g., *Chlamydia trachomatis*) infection [1, 2]. It is defined by a high-yield clinical triad: * **Urethritis** (or cervicitis) [1, 2] * **Conjunctivitis** (or uveitis) [1] * **Arthritis** (typically asymmetric, oligoarticular, and affecting the lower limbs) [1] The mnemonic **"Can't see, can't pee, can't climb a tree"** is frequently used to remember these features. **2. Why the Other Options are Incorrect:** * **Gout:** A crystal-induced arthropathy caused by monosodium urate deposition [3]. It typically presents as acute monoarthritis (Podagra) and does not involve the mucosal surfaces or the urethra. * **Rheumatoid Arthritis (RA):** A chronic systemic inflammatory disorder characterized by symmetric polyarthritis. While it has extra-articular manifestations (e.g., nodules, episcleritis), urethritis is not a feature. * **Polyarteritis Nodosa (PAN):** A systemic necrotizing vasculitis of medium-sized arteries. It commonly involves the kidneys (renal hypertension), skin, and nerves (mononeuritis multiplex), but does not cause primary urethritis. **Clinical Pearls for NEET-PG:** * **HLA-B27 Association:** Approximately 75-90% of patients with Reactive Arthritis are HLA-B27 positive [2]. * **Cutaneous Findings:** Look for **Keratoderma blennorrhagicum** (pustular lesions on palms/soles) and **Circinate balanitis** (painless ulcers on the glans penis) [1]. * **Joint Involvement:** It is the most common cause of non-traumatic inflammatory monoarthritis/oligoarthritis in young adults [1].
Question 80: What is the most common presentation of Wegener's granulomatosis?
- A. Fever
- B. Sinusitis (Correct Answer)
- C. Glomerulonephritis
- D. Diffuse pulmonary infiltrate
Explanation: **Explanation:** **Granulomatosis with Polyangiitis (GPA)**, formerly known as Wegener’s granulomatosis, is a systemic necrotizing vasculitis that typically involves the triad of the upper respiratory tract, lower respiratory tract, and kidneys [1]. **Why Sinusitis is the correct answer:** The **upper respiratory tract** is the most frequently involved site at the time of initial presentation, occurring in over **90% of patients**. Chronic sinusitis is the most common clinical manifestation, often accompanied by nasal crusting, epistaxis, and otitis media. Over time, this can lead to bony destruction, resulting in the classic **saddle-nose deformity**. **Analysis of Incorrect Options:** * **A. Fever:** While constitutional symptoms like fever, weight loss, and malaise are common in systemic vasculitis, they are non-specific and usually secondary to the underlying inflammatory process rather than the primary presenting feature [1]. * **C. Glomerulonephritis:** Renal involvement (Pauci-immune crescentic glomerulonephritis) occurs in about 75–80% of patients during the disease course but is present in only **20% at initial presentation**. It is a major cause of morbidity but not the most common initial sign. * **D. Diffuse pulmonary infiltrate:** Lung involvement occurs in about 85% of cases, typically presenting as **nodules or fixed cavities** rather than diffuse infiltrates (which are more characteristic of Goodpasture syndrome or SLE). **NEET-PG High-Yield Pearls:** * **Serology:** Highly specific for **c-ANCA** (anti-PR3 antibodies). * **Histology:** Characterized by the triad of vasculitis, mucosal granulomas, and geographic necrosis. * **Treatment:** Induction with Corticosteroids + Cyclophosphamide (or Rituximab). * **Limited GPA:** Refers to disease confined to the respiratory tract without renal involvement.
Practice by Chapter
Rheumatoid Arthritis
Practice Questions
Spondyloarthropathies
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Systemic Lupus Erythematosus
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Vasculitis Syndromes
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Scleroderma and Related Disorders
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Inflammatory Myopathies
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Crystal Arthropathies
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Osteoarthritis
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Primary Immunodeficiency Disorders
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Autoinflammatory Syndromes
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Sjögren's Syndrome
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Antiphospholipid Syndrome
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